Nonsteroidal anti-inflammatory drugs arrest growth of cells in the G1 phase of the cell cycle. Growth continues in synchrony once drug is removed. These responses are accompanied by changes in animo acid transport. Active transport by system "A" progressively diminishes and that by system "L" is enhanced; the reverse occurs after removal of drug. Kinetic studies suggest that 1) the changes are due to alteration in the number of carriers rather than in the affinity of carriers for amino acids of Na ion, 2) the decay and recovery of the transport are dependent on turnover of carriers in the plasma membrane, and 3) transport through the "A" system occurred by a "low" and a "high" affinity component; the lattter was prominent during exponential growth and was selectively inhibited by indomethacin. This component was also present in freshly isolated rat thymus lymphocytes and was likewise inhibited by indomethacin whether added directly to cell suspensions or administered (10 mg/kg) prior to isolation of cells.